PF4 drives VSMC proinflammatory response in a KLF4-dependent manner. (A) KLF4 overexpression. HCASMCs were infected with a KLF4-expressing adenovirus (5 and 10 MOI), a control LacZ adenovirus (10 MOI), or were null infected. Controls were also treated with buffer or PF4 (1 µg/mL). Representative KLF4 expression western blot. (B) Overexpression of KLF4 increases IL-6 production (n = 3 ± SD; *P < .01). (C) Inhibition of KLF4 expression decreases IL-6. HCASMCs were treated with scramble control siRNA or KLF4-specific siRNA before PF4. IL-6 was measured by ELISA (n = 3 ± SD; *P < .01). (D) Western blot confirmation of KLF4 knockdown by siRNA. (E) PF4 increases Klf4 expression in vivo. Ligated left carotid Klf4 expression relative to internal control nonligated right carotid was determined by qRT-PCR in WT and PF4^−/− mice (n = 5 ± SD; *P < .05, **P < .01 vs PF4^−/−).